|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our work provides more detail about PKR gene polymorphism in HCV genotype 4a as a new clinical tool for anticipating HCV-4a infection outcome.
|
30080984 |
2019 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
We propose that modulation of autophosphorylation of PKR by p48 isoform is an important mechanism whereby the HCV virus escapes innate antiviral immune responses by circumventing p42-mediated inhibition of its replication.
|
27770702 |
2017 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In fact, activation of pathogen sensors induces the expression of CSR32/EGOT RIG-I and the RNA-activated kinase PKR sense HCV RNA, activate NF-κB and upregulate EGOT EGOT is increased in the liver of patients infected with HCV and after infection with influenza or Semliki Forest virus (SFV).
|
27283940 |
2016 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Treatment with IFN-α increases expression of IFN-stimulated genes (ISGs) such as double-stranded RNA-activated protein kinase (PKR) and decreases viral RNA and protein levels in HCV-infected Huh-7.5 human hepatoma cells.
|
27929099 |
2016 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Finally, we show that NS5A from GBV-C but not from GBV-B down-regulates HCV IRES activity in the absence or the presence of PKR over expression.
|
24815730 |
2014 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Double-stranded RNA-activated protein kinase R (PKR) is known to be upregulated by hepatitis C virus (HCV) and overexpressed in hepatocellular carcinoma (HCC).
|
23844083 |
2013 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Transcriptional response of MxA, PKR and SOCS3 to interferon-based therapy in HCV genotype 4-infected patients and contribution of p53 to host antiviral response.
|
21597279 |
2012 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Novel data points out for a role of PKR as a pro-HCV agent, both as an adapter protein and as an eIF2a-kinase, and in cooperation with the di-ubiquitin-like protein ISG15.
|
23202496 |
2012 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
We report here a detailed study to evaluate the function of PKR in hepatitis C virus genotype 4 (HCV-4) infected patients.
|
22894766 |
2012 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
A PKR/eIF-2α phosphorylation homology domain (PePHD) within the E2 protein has been found to interact with PKR and inhibit PKR in vitro, suggesting a possible mechanism for HCV to evade the antiviral effects of IFN.
|
22270759 |
2012 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Reappraisal of the importance of mutations in the NS5A-PKR-binding domain of hepatitis C-1b virus in the era of optimally individualized therapy.
|
20236237 |
2011 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Double-stranded RNA-activated protein kinase plays an important role in suppressing HCV replication in an innate state, but may not be essential in IFN therapy.
|
19840259 |
2010 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Together, these results demonstrate that PKR is activated by HCV infection and plays a critical antiviral role through inhibition of viral protein translation.
|
19189853 |
2009 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results suggest that the ability of HCV to activate PKR may, paradoxically, be advantageous for the virus during an IFN response by preferentially suppressing the translation of ISGs.
|
20006840 |
2009 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Hepatitis C and evasion of the interferon system: a PKR paradigm.
|
20006836 |
2009 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Sequences within HCV NS5A (PKR binding domain [PKRBD], IFN sensitivity-determining region [ISDR], and variable region 3 [V3]) were analyzed for the pretreatment serum samples of 60 HCV genotype 1-infected patients treated with pegylated IFN plus ribavirin (1b, n = 47; 1a, n = 13) but with different treatment outcomes, those with sustained virologic responses (SVR; n = 36) or nonresponders (NR; n = 24).
|
18448540 |
2008 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
HCV RNA from 50 patients infected with HCV genotype 1b was studied by cloning and sequencing of interferon sensitivity determining region (ISDR), PKR-eIF2alpha phosphorylation homology domain (PePHD).
|
18069766 |
2007 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Significant correlations were found between kinetics of PKR expression and viral decline rates in each phase of hepatitis C virus dynamics (first phase, r = 0.67, P = 0.0006; second phase, r = 0.67, P = 0.001).
|
17501760 |
2007 |
|
Hepatitis C
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
The C-terminal part of E2 (codons 617-711) including PKR/eIF2alpha phosphorylation homology domain (PePHD) and ISDR was sequenced in 85 HCV-1b-infected patients treated by IFN monotherapy.
|
16773689 |
2006 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
The hepatitis C virus (HCV) envelope protein 2 (E2) interacts in vitro with the interferon alpha (IFN-alpha)-inducible double-stranded RNA-activated protein kinase, suggesting a possible mechanism by which HCV may evade the antiviral effects of IFN-alpha.
|
15695675 |
2005 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
PKR protein levels were consistently increased in HCV-related HCC compared with NT (p=0.001); similar increases were seen in total eIF2alpha and the PKR inhibitor p58IPK in T compared with NT (p=0.022, p=0.048, respectively).
|
14638359 |
2003 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Serum hepatitis C viral (HCV) dynamics, double-stranded RNA-activated protein kinase (PKR) mRNA and MxA mRNA levels in peripheral blood mononuclear cells (PBMC) were analyzed serially in 140 patients who were randomly assigned to a twice daily (3 MU bid) or once daily (6 MU qd) administration group.
|
12927929 |
2003 |
|
Hepatitis C
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
Polymorphisms in interferon-induced genes and the outcome of hepatitis C virus infection: roles of MxA, OAS-1 and PKR.
|
12944978 |
2003 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
The double-stranded RNA-activated protein kinase-binding domain (PKRbd) of the NS5A gene of hepatitis C virus (HCV) was studied by the cloning and sequencing method, in HCV-infected patients who had a primary resistance to treatment with interferon (IFN)-alpha (early nonresponders).
|
14593596 |
2003 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
Hepatitis C virus (HCV) E2 protein was recently reported to have a double-stranded RNA-activated protein kinase-eukaryotic initiation factor 2alpha (PKR-eIF2alpha) phosphorylation homology domain (PePHD); PKR is induced by interferon (IFN).
|
12818284 |
2003 |